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Originally published as MBoC in Press, 10.1091/mbc.E09-01-0002 on September 16, 2009

Vol. 20, Issue 22, 4845-4855, November 15, 2009

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Glucose Promotes Stress Resistance in the Fungal Pathogen Candida albicans

Alexandra Rodaki*, Iryna M. Bohovych*, Brice Enjalbert*,{dagger}, Tim Young{ddagger}, Frank C. Odds*, Neil A.R. Gow*, and Alistair J.P. Brown*

*Aberdeen Fungal Group, Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, United Kingdom; and {ddagger}Discovery Biology, Pfizer Ltd, Sandwich, Kent CT13 9NJ, United Kingdom

Submitted January 2, 2009; Revised August 20, 2009; Accepted September 10, 2009
Monitoring Editor: Charles Boone

Metabolic adaptation, and in particular the modulation of carbon assimilatory pathways during disease progression, is thought to contribute to the pathogenicity of Candida albicans. Therefore, we have examined the global impact of glucose upon the C. albicans transcriptome, testing the sensitivity of this pathogen to wide-ranging glucose levels (0.01, 0.1, and 1.0%). We show that, like Saccharomyces cerevisiae, C. albicans is exquisitely sensitive to glucose, regulating central metabolic genes even in response to 0.01% glucose. This indicates that glucose concentrations in the bloodstream (approximate range 0.05–0.1%) have a significant impact upon C. albicans gene regulation. However, in contrast to S. cerevisiae where glucose down-regulates stress responses, some stress genes were induced by glucose in C. albicans. This was reflected in elevated resistance to oxidative and cationic stresses and resistance to an azole antifungal agent. Cap1 and Hog1 probably mediate glucose-enhanced resistance to oxidative stress, but neither is essential for this effect. However, Hog1 is phosphorylated in response to glucose and is essential for glucose-enhanced resistance to cationic stress. The data suggest that, upon entering the bloodstream, C. albicans cells respond to glucose increasing their resistance to the oxidative and cationic stresses central to the armory of immunoprotective phagocytic cells.


This article was published online ahead of print in MBC in Press (http://www.molbiolcell.org/cgi/doi/10.1091/mbc.E09-01-0002) on September 16, 2009.

{dagger}Present address: Unité Mixte de Recherche 5504, Unité Mixte de Recherche 792 Centre National de la Recherche Scientifique, Institut National de la Recherche Agronomique, INSA, ISBP/INSA, 31077 Toulouse, Cedex 4, France.

Address correspondence to: Alistair J.P Brown (al.brown{at}abdn.ac.uk)







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